%0 Figure %A Chu, Tianci %A Zhang, Yi %A Tian, Zhisen %A Ye, Chuyuan %A Zhu, Mingming %A Shields, Lisa %A Kong, Maiying %A Barnes, Gregory %A Shields, Christopher %A Cai, Jun %D 2019 %T MOESM5 of Dynamic response of microglia/macrophage polarization following demyelination in mice %U https://springernature.figshare.com/articles/figure/MOESM5_of_Dynamic_response_of_microglia_macrophage_polarization_following_demyelination_in_mice/10001306 %R 10.6084/m9.figshare.10001306.v1 %2 https://springernature.figshare.com/ndownloader/files/18036608 %K Multiple sclerosis %K Focal demyelination model %K Oligodendrocyte/oligodendrocyte progenitor cells %K Microglia/macrophage %K Neuroinflammation %K Sensorimotor function %K Diffusion tensor imaging %X Additional file 5: Figure S3. Graphic summary of LPC- and LPS-induced distinctive temporal and spatial demyelination patterns. In contrast to LPC-induced robust demyelination with a lag in inflammation/glial response, LPS stimulated strong inflammation/glial response from the early stage and produced diffuse demyelination lesions with its peak demyelination and functional decline later than LPC. OPC/OL, astrocytes, and M/M were scattered throughout the LPS-induced demyelination lesion, but were distributed in a layer-like pattern in the LPC-induced lesion. OPCs populated and migrated into the lesion center to differentiate into mature OLs: OPC/OL were distributed dispersedly in the LPS-induced lesion; while in LPC-induced lesion, OPC/OL were localized in layers around M2. At the late stage, both LPC- and LPS- produced demyelination reached spontaneous remyelination with the restoration of inflammatory niche, a change in M/M subpopulations, and the recruitment/differentiation of OPC/OL into the lesion center. Specific M1/M2 polarization was closely associated with the demyelination-remyelination process, which might be related to the different mechanisms of LPC and LPS in causing inflammation and demyelination. %I figshare